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Rôle Des Facteurs De Transcription NOR1 Et TLE1 Dans Les Macrophages Alternatifs Humains Federica De Paoli

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Rôle Des Facteurs De Transcription NOR1 Et TLE1 Dans Les Macrophages Alternatifs Humains Federica De Paoli Rôle des facteurs de transcription NOR1 et TLE1 dans les macrophages alternatifs humains Federica de Paoli To cite this version: Federica de Paoli. Rôle des facteurs de transcription NOR1 et TLE1 dans les macrophages alternatifs humains. Médecine humaine et pathologie. Université du Droit et de la Santé - Lille II, 2015. Français. NNT : 2015LIL2S006. tel-01257811 HAL Id: tel-01257811 https://tel.archives-ouvertes.fr/tel-01257811 Submitted on 18 Jan 2016 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. UNIVERSITE LILLE NORD DE FRANCE FACULTE DE SCIENCES PHARMACEUTIQUES ET BIOLOGIQUES Thèse Pour obtenir le grade de : DOCTEUR DE L’UNIVERSITE LILLE 2 Spécialité : Biochimie et Biologie Moléculaire Rôle des facteurs de transcription NOR1 et TLE1 dans les macrophages alternatifs humains Presentée et soutenue publiquement par : Federica DE PAOLI Le 25 Février 2015 Directrice de thèse: Dr Giulia CHINETTI-GBAGUIDI Jury: Pr. Bart STAELS, Président Dr. Laurent YVAN-CHARVET, Rapporteur Pr. David MASSON, Rapporteur Dr. Philippe LEFEBVRE, Examinateur Tout est une question d’équilibre REMERCIEMENTS Je tiens tout d’abord à remercier Monsieur le Professeur Bart Staels, qui m’a accueillie au sein de son laboratoire et me fait l’honneur de présider le jury de cette soutenance de thèse. Je l’en remercie sincèrement. Je souhaite adresser ma plus profonde gratitude à ma directrice de thèse Madame le Docteur Giulia Chinetti-Gbaguidi. Je vous remercie pour la confiance que vous m’avez accordée depuis le premier instant. Je tiens à exprimer toute ma reconnaissance pour votre rigueur scientifique, vos précieux conseils, votre soutien et infinie disponibilité ainsi que pour votre présence constante qui n’a jamais cessée malgré les changements logistiques intervenus dans les derniers temps. Je vous serai toujours reconnaissante pour l’énorme bagage scientifique que vous m’avez transmis. E’ stato un onore lavorare con lei e non potrò mai ringraziarla a sufficienza per quanto ho imparato al suo fianco in questi anni. Messieurs le Docteur Laurent Yvan-Charvet et le Professeur David Masson, vous me faites l’honneur d’avoir accepté de juger ce travail et d’en être les rapporteurs. Je vous prie de trouver ici le témoignage de ma reconnaissance et mon profond respect. Monsieur le Docteur Philippe Lefebvre, je suis honorée de votre présence dans mon jury de thèse en qualité d’examinateur. Recevez ici mes sincères remerciements. Je remercie Jérôme pour sa disponibilité et son professionnalisme, j’ai apprecié travailler avec toi au cours des ces années. Je tiens à exprimer un immense merci à tous les gens du labo, de Pasteur à J&K pour leur sympathie. Une mention spéciale à Christian pour les tonnes de gel shift et de plasmides clonés, les bons conseils, les petites blagues et pour m’avoir aidée à relativiser les choses :-), Corinne C pour ta rigueur en salle de culture, Bruno pour les milliards de Q-PCR, à Sophie et Yasmine, correctrices officielles de la forme de ce manuscrit, à Mehdi, mon collègue « fou » de bureau, à Benoit, Jonathan, Steve, Denis, Gael, Stephane, Corinne R, Isa et Barbara pour vos suggestions, vos sourires et votre soutien. Je l’ai beaucoup apprécié ! 3 Un super grand merci (GRAZIE) à Mél ( !!), Loïc et Geoffrey pour vos blagues, le grand aide et pour avoir fait preuve de courage à tolérer mon sacré caractère, heureusement que « par fois » vous étiez la:-P Un immense merci à ceux que j’ai croisé dans les couloirs de ce labo et que avec le temps sont devenus mes amis dans cette vie française : Yoanna, Vera, Morgane et Michal. LN, merci pour nos entraînements sportifs, divisés entre la course à pied dans les soirées glaciales d’hiver et les bains dans l’eau chlorée des piscines lilloises pour déteindre les nerves. Manju, it was a big chance to meet you! Thanks a lot for having initiated me to indian food, by the way I still prefer when you add sugar instead of spicies :-P Merci à Marta et Clement pour avoir rendu les années lillloises amusantes, riches en rencontre et folles à la juste mésure. Un grazie di cuore alla mia famiglia per non avermi mai fatto mancare supporto e calore in questi anni lontana da casa. Grazie grazie grazie ai miei amici di sempre che nonostante le “interruzioni di segnale” di skype e whatsap mi sono sempre stati vicini, mi hanno motivata, compresa e regalato una risata: Manu, Sara-Clara, Davide, Roby, Melissa, Anita, Claudia, Fiocco. Comment oublier Sami et Vale, parce que nous sommes « tous dans le même bateau ». Sami merci pour m’avoir accompagnée dans mes délires comme le saut à l’élastique ! La prochaine épreuve : saut en parachute ! Vale cosa fare io senza di te ? Sei la miglior compagna di avventura ed Amica che avrei mai potuto desiderare!! Grazie di cuore per tutto :-) 4 LISTE DES PUBLICATIONS Publications originales De Paoli F, Eeckhoute J, Copin C, Vanhoutte J, Duhem C, Derudas B, Dubois-Chevalier J, Colin S, Zawadzki C, Jude B, Haulon S, Lefebvre P, Staels B, Chinetti-Gbaguidi G. The neuron-derived orphan receptor 1 (NOR1) is induced upon human alternative macrophage polarization and stimulates the expression of markers of the M2 phenotype. Atherosclerosis 2015 (en revision favorable). Vinod M, Chennamsetty I, Colin S, Belloy L, De Paoli F, Schaider H, Graier WF, Frank S, Kratky D, Staels B, Chinetti-Gbaguidi G, Kostner GM. miR-206 controls LXRα expression and promotes LXR-mediated cholesterol efflux in macrophages. Biochim Biophys Acta 2014; 1841(6): 827-35. Article de synthèse De Paoli F, Staels B, Chinetti-Gbaguidi G. Macrophage phenotypes and their modulation in atherosclerosis. Circulation Journal 2014; 78(8):1775-81. COMMUNICATIONS ORALES ET AFFICHEES De Paoli F, Eeckhoute J, Copin C, Vanhoutte J, Derudas B, Chevalier J, Zawadzki C, Jude B, Haulon S, Pattou F, Lefebvre P, Staels B, Chinetti-Gbaguidi G. The Neuron-derived orphan receptor 1 (NOR1) is induced upon human alternative macrophage polarization and stimulates markers of the M2 phenotype. 10ème congrès de la NSFA (Nouvelle Société Française d’Athérosclérose), Biarritz , 19-21 juin 2014. Communication affichée, obtention du prix poster. De Paoli F, Eeckhoute J, Copin C, Vanhoutte J, Derudas B, Chevalier J, Zawadzki C, Jude B, Haulon S, Pattou F, Lefebvre P, Staels B, Chinetti-Gbaguidi G. Control of macrophage polarization by NOR1. Journée Think Tank 2014, Lille, 26 juin 2014. Communication orale De Paoli F, Copin C, Vanhoutte J, Zawadzki C, Jude B, Haulon S, Eeckhoute J, Lefebvre P, Staels B, Chinetti-Gbaguidi G. The neuron-derived orphan nuclear receptor 1 (NOR1) is induced in human alternative macrophages and controls the expression of alternative polarization markers. 81ème congrès de l’EAS (European Atherosclerosis Society), Lion, 2-5 juin 2013. Communication affichée 5 De Paoli F, Copin C, Vanhoutte J, Zawadzki C, Jude B, Haulon S, Eeckhoute J, Lefebvre P, Staels B, Chinetti-Gbaguidi G. The neuron-derived orphan nuclear receptor 1 (NOR1) is induced in human alternative macrophages and controls the expression of alternative polarization markers. FEBS Advanced Lecture Course, Spetses summer school on nuclear receptor signalling in physiology and disease, Ile de Spetses (Grece), 25-30 aout 2013. Communication affichée De Paoli F, Copin C, Vanhoutte J, Zawadzki C, Jude B, Haulon S, Eeckhoute J, Lefebvre P, Staels B, Chinetti-Gbaguidi G. The neuron-derived orphan nuclear receptor 1 (NOR1) is induced in human alternative macrophages and controls the expression of alternative polarization markers. 12ème journée André Verbert, Lille, 11 septembre 2012. Communication affichée FINANCEMENT Bourse doctorale de l’Université Lille 2 accordée pour les 3 année de thèse FORMATIONS SUIVIES Bien utiliser les indicateurs bibliometriques en biologie-santé (facteur d’impact, h-index, sigaps) du 16 octobre 2014 Doc’Emploi du 13 novembre 2014 Guided Microarray data analysis (Partek) du 12 septembre 2013 Séminaire Athérosclérose: Nutrition et prevention du risque cardiovasculaire, 20-22 septembre 2012 6 RESUME Etude de l’expression et du rôle de NOR1 dans les macrophages alternatifs humains NOR1 (NR4A3) avec deux autres membres, Nurr1 et Nur77, fait partie de la famille des récepteurs nucléaires NR4A. Les trois récepteurs sont exprimés par les macrophages au sein de la lésion d’athérosclérose humaine. Cependant, l’expression et le rôle de NOR1 dans les macrophages alternatifs n’ont pas encore été étudiés. En utilisant le modèle in vitro de macrophages primaires alternatifs humains polarisés en présence d’IL-4, nous avons démontré que l’expression de NOR1 est induite dans les macrophages M2, une régulation pas observée chez la souris. D’ailleurs, l’expression de NOR1 est plus importante dans les zones de la lésion athérosclérotique humaine enrichies en macrophages alternatifs CD68+MR+. En utilisant l’approche de diminution de l’expression de NOR1 par un siRNA spécifique, nous démontrons que l’expression de certains marqueurs de la polarisation alternative tels que Mannose Receptor (MR), Interleukin-1 receptor antagonist (IL1Ra), CD200 receptor (CD200R), coagulation factor XIII A1 polypeptide (F13A1), interleukin 10 (IL10) et Peroxisome Proliferator- Activated Receptor (PPAR) est diminuée. Des analyses bioinformatiques ont identifié les gènes F13A1, IL-1Ra, IL-10 et la matrix metallopeptidase 9 (MMP9), comme étant des cibles potentielles de NOR1 dans les macrophages alternatifs humains. De plus, l’expression et l’activité enzymatique de la MMP9 sont induites suite au silencing de NOR1, une régulation confirmée par l’approche de surexpression de NOR1 par infection adénovirale.
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